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What does Dr. Dake have to say about MRI flow quantification? I did not know he was involved in this.

I am not overly optimistic for MRI technology in CCSVI. It just seems like hitting a nail with a sledgehammer when a regular hammer would do. There is an advantage in its noninvasiveness but I've yet to see good data showing concordance between what is seen on MRV and what is seen on venogram, and especially on venogram and IVUS together.

Another good set of three speakers. Dr. Zivadinov has done over two years of research on CCSVI at BNAC. We discussed Dr. Hu earlier in this thread, and along with Dr. Chung, he is the doctor who had researched jugular venous reflux in transient global amnesia. But it's Dr. Cooke's presentation that is of most interest to me, since it gets at a possible explanation for the blood-brain barrier permeability in MS, which is a direct path from the jugular blockages and turbulent flow of CCSVI to the weakened blood-brain barrier with increased adhesion molecules that pulls over greater numbers of leukocytes into the brain, thus leading to the immune system involvement in MS. You all have seen the image of the effects of shear stress but it's a good one:

The turbulent hemodynamics as seen in the second image would lead to an increase in endothelium adhesion and permeability. The particular endothelium of interest is the lining of the capillaries of the brain, aka the blood brain barrier.

Hi Cece--Dr. Dake is quite knowledgable on MRV, and admits it is an art. As Dr. Zamboni has mastered doppler US, MRV is Dr. Dake and Dr. Haacke's milleu. He presented on his findings at the last ISNVD meeting.

Dr. Michael Dake presented for Dr. C.J. Elkins on the role of 3D flow quantification in studying abnormal flow characteristics. This technique offers much larger coverage than the 2D methods and opens the door to a global study of the fluid dynamics of the head/neck system. He also noted a particular bimodal cardiac flow characteristic in the flow pattern of MS patients.

Because Dr. Dake is a cardiac specialist and IR, he has noted things that the other doctors might have missed--like an unusual cardiac flow characteristic. Flow quantification is a huge part of this puzzle, and only elucidated by MRV. If hypoperfusion turns out to be the biomarker for MS, it will be because of MRV flow quantifications. Each doctor brings the wealth of their experience and knowledge to the table. I'm thrilled that the endothelium, sheer stress, hypoperfusion and hypoxia are being looked at in the CCSVI model, and that Dr. Cooke remains involved in the research. Should be a terrific conference next February! For those that are interested in attending the Patient Day (in person or on the web) here's info:http://www.isnvd.org/index.php?site=patientday#contentcheer

INVITED SPEAKERS Raj Attariwala, CANADAI have bolded everyone I feel reasonably familiar with, but that leaves a lot of unbolded names. If you know anything interesting about the unbolded names, or the bolded ones, please share. It is not too early to get excited about ISNVD.

Dr. Raj Attariwala, MD PhD FRCPC FANM works for AIM Medical Imaging in Vancouver, BC. He was one of our conference speakers on September 10. His PhD is in Fluid Dynamics and he is a radiologist on top of that. He developed a way to measure CCSVI using a custom built MRI. He spent 4 hours with me describing his research and ideas -- he definately is keen to contribute his understanding to this new discovery. There's a lot of debate over whether an MRI has to follow the Haacke protocol, but IMO, I would take either Dr. Attariwala or Dr. Haacke's images and interpretations any day. These two researchers work together, but they met for the first time at our conference.

Some interesting memories from our lengthy conversation:- Raj said any doctor presented with the evidence he has seen would not be able to deny CCSVI - He cautioned we are trying to do in 2 years what usually takes the medical system 20 years- He says some lesions are the result of fluids moving energy through the system, basically, an echo, that damages the smallest capilliaries of the brain- He claims the degree of stenosis doesn't matter -- a 5% stenosis can create a more devastating echo than a 50% one- He wants engineers involved in predicting how and where damage will occur (he is also an engineer)

cheerleader wrote:Hi Cece--Dr. Dake is quite knowledgable on MRV, and admits it is an art. As Dr. Zamboni has mastered doppler US, MRV is Dr. Dake and Dr. Haacke's milleu. He presented on his findings at the last ISNVD meeting.

Dr. Michael Dake presented for Dr. C.J. Elkins on the role of 3D flow quantification in studying abnormal flow characteristics. This technique offers much larger coverage than the 2D methods and opens the door to a global study of the fluid dynamics of the head/neck system. He also noted a particular bimodal cardiac flow characteristic in the flow pattern of MS patients.

Because Dr. Dake is a cardiac specialist and IR, he has noted things that the other doctors might have missed--like an unusual cardiac flow characteristic. Flow quantification is a huge part of this puzzle, and only elucidated by MRV. If hypoperfusion turns out to be the biomarker for MS, it will be because of MRV flow quantifications. Each doctor brings the wealth of their experience and knowledge to the table. I'm thrilled that the endothelium, sheer stress, hypoperfusion and hypoxia are being looked at in the CCSVI model, and that Dr. Cooke remains involved in the research. Should be a terrific conference next February! For those that are interested in attending the Patient Day (in person or on the web) here's info:http://www.isnvd.org/index.php?site=patientday#contentcheer

I hold Dr. Dake in high esteem, so I am interested in anything that he presents. Do you know what is meant by a particular bimodal cardiac flow in the flow patterns of MS patients? Is this something that goes away after CCSVI treatment?

Summary of the consensus on catheter venography and IVUS (Salvatore Sclafani, USA)

Summary of the consensus on US imaging standards (Nikolaos Liasis, Greece)

Dr. Raj Attariwala is definitely attending, since he is involved in a consensus breakout session and in summarizing the consensus on an MRI CCSVI protocol. I can see how we are trying to do in two years what would normally take twenty, but what a shame that it takes that long normally.

I am curious about the impact of degree of stenosis. Even after treatment, we might be left with stenoses, hopefully of lower percentiles such as 5%, because angioplasty is not always 100% successful.

Thanks for the background on Dr. Attariwala. One more off the list!

(Dr. Sclafani is in there right after Dr. Attariwala. I am not sure what is meant by establishing IVUS imaging standards. I expect it is technical? This is not about whether or not to use IVUS, but how to use it if you do? I am all for standardization, and establishing what is best, and IVUS.)

Dr. Attariwala had given an excellent presentation on Fluid Dynamics in relation to CCSVI at the New Discoveries, New Beginnings forum held on Vancouver Island in September under the sponsorship of the NCS (http://www.facebook.com/nationalccsvisociety). There is a 3 disc set available from NCS which includes all of the presentations. Sandra, you might want to jump in here and bump how to obtain copies of this great set of presentations. Incidentally, Sandra, you did a great job in organizing both the Island show and that tremendous Global CCSVI Expo. I hope you are recovering from all the efforts required.

I spent about 4 hours with Dr. Attariwala last month talking about fluid dynamics in relation to CCSVI and discussion of MRI flow quantification as a means to gain greater insights into fluid dynamics and pressure distribution - with possible repurcussions in hypertension, hypoperfusion and hypoxia. In overview Dr. Attariwala and I are (I hope I am not mis-representaing you here Raj) are on about the same page in the relationships between venous reflux and its possible consequences.

ttucker3 wrote:I spent about 4 hours with Dr. Attariwala last month talking about fluid dynamics in relation to CCSVI and discussion of MRI flow quantification as a means to gain greater insights into fluid dynamics and pressure distribution - with possible repurcussions in hypertension, hypoperfusion and hypoxia. In overview Dr. Attariwala and I are (I hope I am not mis-representaing you here Raj) are on about the same page in the relationships between venous reflux and its possible consequences.

When I first heard of CCSVI back in late 2009, it was something that had been discussed here at TiMS since 2008 and obviously was known about in Italy and at Stanford and in Brooklyn and at BNAC and Poland, and that was about it. Now I am racing to keep up with all the names, and in different fields, of the doctors and researchers who are coming together to share what they are learning.

I need to learn more about flow quantification in MRI, if Dr. Attariwala and yourself see a role for it in illuminating aspects of the fluid dynamics and pressure or focal hypertension points in CCSVI patients.

From the top! Here is a consensus session on ultrasound as a screening method. Dr. Simka's study comparing ultrasound and angiography might further clarify whether ultrasound is reliable. Dr. Menegatti asks if thoracic pump influences cerebral venous return, and of course it does, but does this affect ultrasound screening? What is Dr. Viselner finding when screening for CCSVI in other neurological diseases? Dr. Zamboni's original research did not find CCSVI in other neurological diseases, but Dr. Zivadinov's research did. Karen Marr is the Doppler Ultrasound Unit Director at Buffalo Neuroimaging Analysis Center. I believe Angela Lagace is the sonographer who works with Dr. Sandy MacDonald?

Dr. Hewett of Synergy in California is presenting on MRI CCSVI protocol. I am not sure what Dr. Zivadinov means by morphological MRV multimodal studies. Morphological, multimodal? Someone help me out. There is Dr. Dake, who we have established is quite knowledgeable on MRV, talking about flow quantification. Dr. Haacke is talking about the MS MRI database. I believe he is in need of healthy controls to compare the many MS patient MRVs that he has done. Last but in no way least, there is Dr. Zamboni himself, speaking on multi-modality comparison. There we are talking multimodal again. This must mean studies done with MRV and ultrasound, or MRV and angiography.

We were talking about Ms. Rowling and Harry Potter recently. In one of the books, Hermione signed up for multiple classes all offered at the same time, and managed to attend them all.... But in the real world, we'd have to choose. I'd say 'Catheter venography and IVUS imaging standards' is the stand-out, and not because Dr. Sclafani is giving that one (although that doesn't hurt) but because the combination of catheter venogram and intravascular ultrasound is the most possible information that can currently be had.

Ok, looking up Sturge Weber disease again.http://www.sturge-weber.org/about-sws/c ... drome.htmlIt affects the brain and eyes. An overabundance of capillaries make for a port wine stain on the face, and excessive blood vessel growth on the surface of the brain lead to neurological issues.

Dr. Juhász’s research interests are in functional and structural neuroimaging of epilepsy, brain tumors and developmental brain disorders, with a particular interest in the pathophysiology and progression of Sturge-Weber syndrome. He performed extensive research applying multimodal neuroimaging, combining magnetic resonance imaging techniques with PET imaging using various radiotracers to measure brain glucose metabolism, benzodiazepine receptor binding and tryptophan metabolism. He has also combined these techniques with EEG to improve localization of epileptic foci in patients with medically uncontrolled epilepsy and provides multimodal imaging support to the pediatric epilepsy surgery program at CHM. Dr. Juhász is the principal investigator of several grant projects funded by the National Institutes of Health to study progression of brain structural and functional abnormalities in Sturge-Weber syndrome and to explore the clinical use of tryptophan PET imaging in the detection and monitoring of brain tumors and extracerebral cancers

Could we do PET imaging using radiotracers to measure brain glucose metabolism in CCSVI? If there were changes from before CCSVI treatment compared to after CCSVI treatment, that might be relevant. It might only be of use in the study of epilepsy, I don't know?http://www.ncbi.nlm.nih.gov/pmc/articles/PMC557957/

This work demonstrated that perfusion MR deficits correlate with the severity of neurologic impairment in SWS indicating that it will likely be useful for tracking response to treatment in a clinical trial and neurologic progression.

In SWS, PWI indicates cerebral hypoperfusion predominantly due to impaired venous drainage, with only the most severely affected regions in some patients also showing arterial perfusion deficiency. The extent and severity of the perfusion abnormality and neuronal loss/dysfunction reflect the severity of neurological symptoms and disability, and the highest correlation is found with the degree of hemiparesis.

What's that? Impaired venous drainage can lead to cerebral hypoperfusion, and the extent of the hypoperfusion will reflect the severity of neurological symptoms? That is very relevant to what we are seeing in CCSVI. http://www.ncbi.nlm.nih.gov/pubmed/18056693

Decreased arterial flow velocity and increased pulsatility index in the middle cerebral artery and posterior cerebral artery suggests a high resistance pattern that may reflect venous stasis and may contribute to chronic hypoperfusion of brain tissue.

We report the case of a 9-month-old boy with Sturge-Weber syndrome and new onset of seizure. Perfusion MR imaging showed early changes compatible with impaired venous drainage in the affected hemisphere, whereas proton MR spectroscopic imaging revealed a focal parietal area of elevated choline without significant alteration of N-acetylaspartate levels.

Again, impaired venous drainage.

Fibronectin, which is critical in angiogenesis and blood vessel development, is abnormally expressed in Sturge-Weber syndrome; in CCSVI, fibronectin is presumably normal.

Boston Urine Testing

The purpose of this study is to determine if urine vascular factors in SWS can help us understand more about the pathogenesis of SWS and whether it can be used to monitor response to treatment or predict outcome.

This study is measuring blood vessel factors in the urine of individuals with Sturge-Weber syndrome in collaboration with the laboratory of Dr. Marsha Moses. Urine vascular biomarkers have been developed for other vascular malformations to monitor response to treatment or predict disease severity and we are working on similar progress with Sturge-Weber syndrome.

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